Heteropodatoxin-1

Non Antibodies

Proteins

Israel

Storage as Solution: The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles. - Storage before Reconstitution: The product is shipped as a lyophilized powder at room temperature. Upon receipt, store the product at -20°C. Protect from moisture. - Storage after Reconstitution: The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles.

Lyophilized

Kappa-sparatoxin-Hv1a, Kappa-SPRTX-Hv1a, HpTX1, Toxin AU3/KJ5 - An activator of Nav1.9 and an inhibitor of Kv4.2 and Nav1.7

An activator of Nav1.9 and an inhibitor of Kv4.2 and Nav1.7

12352202

Disulfide bonds between: Cys²-Cys¹⁷, Cys⁹-Cys²², Cys¹⁶-Cys²⁷

Trp³³ - C-terminal amidation

Heteropodatoxin-1, first identified as an inhibitor of Kv4.2 voltage gated potassium channel, also inhibits Nav1.7 and activates Nav1.9 channels, but does not affect Nav1.8 channels.

no

Heteropodatoxin-1 (HpTX1 or kappa-sparatoxin-Hv1a) is a peptide toxin originally isolated from Heteropoda venatoria, a spider species that is mostly present in tropical regions of the world. This toxin belongs to the Heteropoda toxins family that includes HpTX1, HpTX2 and HpTX3, all of which were shown to be Kv4.2 voltage gated potassium channel inhibitors1.Recently it has been found that HpTX1 is a Nav channel pharmacological tool as well. HpTX1 inhibits Nav1.7 and activates Nav1.9, but has no effect on Nav1.8 channel2.The voltage-gated sodium channels Nav1.7, Nav1.8 and Nav1.9, preferentially expressed in the peripheral terminals of sensory neurons and are critical for pain perception in peripheral nociceptors3. Loss of function of Nav1.7 leads to congenital insensitivity to pain in humans2. Genetic and functional studies have illustrated that mutations in Nav1.8 and Nav1.9 cause human pain disorders, providing direct clinical evidence linking these two channels to human pain. Considering that the three channels play distinct roles in the generation and propagation of action potentials, they might regulate pain signaling cooperatively. HpTx1-induced hypersensitivity is mediated by Nav1.9 activation and offers pharmacological insight into the relationship of the three Nav channels in pain signaling2.